tbuckley/cabot-search huggingface dataset:
Temporal Trends in Noncardiovascular Morbidity and Mortality Following Acute Myocardial Infarction
Authors: Daniel Mølager Christensen, Jarl Emanuel Strange, Mohamad El-Chouli, Alexander Christian Falkentoft, Morten Malmborg, Nina Nouhravesh, Gunnar Gislason, Morten Schou, Christian Torp-Pedersen, Thomas S.G. Sehested
Journal: Journal of the American College of Cardiology (2023)
Mortality Trends After Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction
Authors: Pernille Gro Thrane, Kevin Kris Warnakula Olesen, Troels Thim, Christine Gyldenkerne, Martin Bødtker Mortensen, Steen Dalby Kristensen, Michael Maeng
Journal: Journal of the American College of Cardiology (2023)
Recent progress of self-immobilizing and self-precipitating molecular fluorescent probes for higher-spatial-resolution imaging
Authors: Jiawei Yan, Huanying Liu, Yingxu Wu, Ben Niu, Xiaojing Deng, Linhao Zhang, Qi Dang, Yubo Wang, Xiao Lu, Boyu Zhang, Wen Sun
Journal: Biomaterials (2023)
Filling the gap: investigating the interpretability of the Recap of atopic eczema questionnaire
Authors: Robert F Ofenloch
Journal: British Journal of Dermatology (2023)

Journal Article Filling the gap: investigating the interpretability of the Recap of atopic eczema questionnaire Get access Robert F Ofenloch Robert F Ofenloch Conceptualization Section of Occupational Dermatology, Department of Dermatology, University Hospital, Ruprecht-Karl University of Heidelberg, Germany Email: robert.ofenloch@med.uni-heidelberg.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 189, Issue 5, November 2023, Pages 506–507, https://doi.org/10.1093/bjd/ljad287 Published: 09 August 2023 Article history Received: 04 August 2023 Published: 09 August 2023 Corrected and typeset: 09 September 2023
Single-tunnel Zenker’s diverticulum peroral endoscopic myotomy
Authors: Georgios Mavrogenis, Efthymios Maurommatis, Charalampos Koumentakis, Ioannis Tsevgas, Dimitrios Zachariadis, Fateh Bazerbachi
Journal: Endoscopy (2023)

Zenker’s diverticulum peroral endoscopic myotomy (zPOEM) revolutionized the endoscopic treatment of Zenker’s diverticulum, since this is the only method that can provide deep myotomy [1]. Historically, the mucosal entrance was initially made in the hypopharynx, proximal to the septum. The procedure was recently modified [2], and many endoscopists have adapted this latest variation of mucosal entrance over the septum. In this video ([Video 1]), we present a new modification of this technique with the creation of a single tunnel instead of two. In particular, after mucosal incision over the septum ([Fig. 1]), a submucosal cushion is created at the esophageal side and a single tunnel is created at the side of the diverticulum ([Fig. 2], [Fig. 3]). Partial myotomy is performed, if necessary, to open the space for tunneling. Then, myotomy is performed through the diverticular tunnel ([Fig. 4], [Fig. 5]). This harbors the danger of damaging the esophageal mucosa. Therefore, repeated injections are provided at the submucosal space between the septum and the mucosa of the esophagus as needed. In our experience, this modification reduces the total duration of the procedure. The main potential drawback is the risk of inadvertent esophageal mucosal injury if the submucosal cushion is not sufficient.
Histopathologic uncertainties after colorectal endoscopic submucosal dissection with visible retraction of proper muscle layer
Authors: Andrej Wagner, Daniel Neureiter, Frieder Berr
Journal: Endoscopy (2023)

See also: Histological R0 classification after colorectal endoscopic submucosal dissection: a gold standard with feet of clayEndoscopy 2022; 54(S 02): E798-E799DOI: 10.1055/a-1816-7853 See also: Reply to Wagner et al.Endoscopy 2023; 55(09): 885-885DOI: 10.1055/a-2066-8367
EEF2-inactivating toxins engage the NLRP1 inflammasome and promote epithelial barrier disruption
Authors: Miriam Pinilla, Raoul Mazars, Romain Vergé, Leana Gorse, Margaux Paradis, Bastien Suire, Karin Santoni, Kim Samirah Robinson, Gee Ann Toh, Laure Prouvensier, Stephen Adonai Leon-Icaza, Audrey Hessel, David Péricat, Marlène Murris, Hélène Guet-Revillet, Anthony Henras, Julien Buyck, Emmanuel Ravet, Franklin L. Zhong, Céline Cougoule, Rémi Planès, Etienne Meunier
Journal: The Journal of Experimental Medicine (2023)

Human airway and corneal epithelial cells, which are critically altered during chronic infections mediated by Pseudomonas aeruginosa, specifically express the inflammasome sensor NLRP1. Here, together with a companion study, we report that the NLRP1 inflammasome detects exotoxin A (EXOA), a ribotoxin released by P. aeruginosa type 2 secretion system (T2SS), during chronic infection. Mechanistically, EXOA-driven eukaryotic elongation factor 2 (EEF2) ribosylation and covalent inactivation promote ribotoxic stress and subsequent NLRP1 inflammasome activation, a process shared with other EEF2-inactivating toxins, diphtheria toxin and cholix toxin. Biochemically, irreversible EEF2 inactivation triggers ribosome stress–associated kinases ZAKα- and P38-dependent NLRP1 phosphorylation and subsequent proteasome-driven functional degradation. Finally, cystic fibrosis cells from patients exhibit exacerbated P38 activity and hypersensitivity to EXOA-induced ribotoxic stress–dependent NLRP1 inflammasome activation, a process inhibited by the use of ZAKα inhibitors. Altogether, our results show the importance of P. aeruginosa virulence factor EXOA at promoting NLRP1-dependent epithelial damage and identify ZAKα as a critical sensor of virulence-inactivated EEF2.
Diphtheria toxin activates ribotoxic stress and NLRP1 inflammasome-driven pyroptosis
Authors: Kim Samirah Robinson, Gee Ann Toh, Muhammad Jasrie Firdaus, Khek Chian Tham, Pritisha Rozario, Chrissie K. Lim, Ying Xiu Toh, Zhi Heng Lau, Sophie Charlotte Binder, Jacob Mayer, Carine Bonnard, Florian I. Schmidt, John E.A. Common, Franklin L. Zhong
Journal: The Journal of Experimental Medicine (2023)

The ZAKα-driven ribotoxic stress response (RSR) is activated by ribosome stalling and/or collisions. Recent work demonstrates that RSR also plays a role in innate immunity by activating the human NLRP1 inflammasome. Here, we report that ZAKα and NLRP1 sense bacterial exotoxins that target ribosome elongation factors. One such toxin, diphtheria toxin (DT), the causative agent for human diphtheria, triggers RSR-dependent inflammasome activation in primary human keratinocytes. This process requires iron-mediated DT production in the bacteria, as well as diphthamide synthesis and ZAKα/p38-driven NLRP1 phosphorylation in host cells. NLRP1 deletion abrogates IL-1β and IL-18 secretion by DT-intoxicated keratinocytes, while ZAKα deletion or inhibition additionally limits both pyroptotic and inflammasome-independent non-pyroptotic cell death. Consequently, pharmacologic inhibition of ZAKα is more effective than caspase-1 inhibition at protecting the epidermal barrier in a 3D skin model of cutaneous diphtheria. In summary, these findings implicate ZAKα-driven RSR and the NLRP1 inflammasome in antibacterial immunity and might explain certain aspects of diphtheria pathogenesis.
Hormone Receptor–Positive Breast Cancer Sensitive to Pembrolizumab: Evidence of the Pathogenicity of the MLH1 Variant 1835del3
Authors: Henry G. Kaplan, Jeffrey R. Whiteaker, Brianna Nelson, Richard G. Ivey, Travis D. Lorentzen, Uliana Voytovich, Lei Zhao, David J. Corwin, Robert Resta, Amanda G. Paulovich
Journal: Journal of the National Comprehensive Cancer Network (2023)

A woman with estrogen/progesterone receptor-positive, ERBB2-negative metastatic breast cancer developed progressive disease despite treatment with multiple hormonal and chemotherapeutic modalities. She carried a germline variant of MLH1 (1835del3), also known as c.1835_1837del and v612del, the pathogenicity of which has not been conclusively determined. MLH1 staining was not seen on immunohistochemical staining of her tumor tissue. The patient experienced a >5-year dramatic response to 4 doses of pembrolizumab. Family studies revealed multiple other relatives with the MLH1 1835del3 variant, as well as multiple relatives with colon cancer. The one relative with colon cancer who underwent genetic testing demonstrated the same variant. Laboratory studies revealed that the patient's tumor showed loss of heterozygosity (LOH) in the MLH1 region, high levels of microsatellite instability, and a high tumor mutational burden. LOH in the MLH1 region, along with the remarkable clinical response to pembrolizumab treatment and the presence of the same MLH1 variant in affected relatives, supports the hypothesis that the MLH1 1835del3 variant is pathogenic. Given the patient's family history, this likely represents an uncommon presentation of Lynch syndrome. Physicians should be alert to evaluate patients for targetable genetic variants even in unlikely clinical situations such as the one described here.
Breaching the stalemate on assisted dying: it’s time to move beyond a medicalised approach
Authors: Nancy Preston, Sheila Payne, Suzanne Ost
Journal: BMJ (2023)

Despite growing legal and medical support for assisted dying, many healthcare professionals do not want to be directly involved. Could a de-medicalised approach help to overcome this? <b>Nancy Preston</b>, <b>Sheila Payne</b>, and <b>Suzanne Ost</b> discuss
Dynamic Stiffening Hydrogel with Instructive Stiffening Timing Modulates Stem Cell Fate In Vitro and Enhances Bone Remodeling In Vivo
Authors: Xiaomeng Li, Shuaibing Liu, Shanshan Han, Qingqing Sun, Jianmin Yang, Yuhang Zhang, Yongchao Jiang, Xiaofeng Wang, Qian Li, Jianglin Wang
Journal: Advanced Healthcare Materials (2023)

Biomechanical stimuli derived from the extracellular matrix (ECM) extremely tune stem cell fate through 3D and spatiotemporal changes in vivo. The matrix stiffness is a crucial factor during bone tissue development. However, most in vitro models to study the osteogenesis of mesenchymal stem cells (MSCs) are static or stiffening in a 2D environment. Here, a dynamic and controllable stiffening 3D biomimetic model is created to regulate the osteogenic differentiation of MSCs with a dual-functional gelatin macromer that can generate a double-network hydrogel by sequential enzymatic and light-triggered crosslinking reactions. The findings show that these dynamic hydrogels allowed cells to spread and expand prior to the secondary crosslinking and to sense high stiffness after stiffening. The MSCs in the dynamic hydrogels, especially the hydrogel stiffened at the late period, present significantly elevated osteogenic ECM secretion, gene expression, and nuclear localization of Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ). In vivo evaluation of animal experiments further indicates that the enhancement of dynamic stiffening on osteogenesis of MSCs substantially promotes bone remodeling. Consequently, this work reveals that the 3D dynamic stiffening microenvironment as a critical biophysical cue not only mediates the stem cell fate in vitro, but also augments bone restoration in vivo.
Impact of Gestational Diabetes Detection Thresholds on Infant Growth and Body Composition: A Prospective Cohort Study Within a Randomized Trial
Authors: Komal Manerkar, Caroline A. Crowther, Jane E. Harding, Michael P. Meyer, Cathryn A. Conlon, Elaine C. Rush, Jane M. Alsweiler, Lesley M.E. McCowan, Janet A. Rowan, Richard Edlin, Francesca Amitrano, Christopher J.D. McKinlay
Journal: Diabetes Care (2023)

Gestational diabetes mellitus (GDM) is associated with offspring metabolic disease, including childhood obesity, but causal mediators remain to be established. We assessed the impact of lower versus higher thresholds for detection and treatment of GDM on infant risk factors for obesity, including body composition, growth, nutrition, and appetite.In this prospective cohort study within the Gestational Diabetes Mellitus Trial of Diagnostic Detection Thresholds (GEMS), pregnant women were randomly allocated to detection of GDM using the lower criteria of the International Association of Diabetes and Pregnancy Study Groups or higher New Zealand criteria (ACTRN12615000290594). Randomly selected control infants of women without GDM were compared with infants exposed to A) GDM by lower but not higher criteria, with usual treatment for diabetes in pregnancy; B) GDM by lower but not higher criteria, untreated; or C) GDM by higher criteria, treated. The primary outcome was whole-body fat mass at 5-6 months.There were 760 infants enrolled, and 432 were assessed for the primary outcome. Fat mass was not significantly different between control infants (2.05 kg) and exposure groups: A) GDM by lower but not higher criteria, treated (1.96 kg), adjusted mean difference (aMD) -0.09 (95% CI -0.29, 0.10); B) GDM by lower but not higher criteria, untreated (1.94 kg), aMD -0.15 (95% CI -0.35, 0.06); and C) GDM detected and treated using higher thresholds (1.87 kg), aMD -0.17 (95% CI -0.37, 0.03).GDM detected using lower but not higher criteria, was not associated with increased infant fat mass at 5-6 months, regardless of maternal treatment. GDM detected and treated using higher thresholds was also not associated with increased fat mass at 5-6 months.
Endoscopy International Open – recently published
Journal: Endoscopy (2023)

Comment on: EUS-guided transcolonic drainage and necrosectomy in walled-off necrosis: a retrospective, single-center case seriesEndosc Int Open 2023; 11(06): E618-E622DOI: 10.1055/a-2095-0272 Comment on: Long-term outcomes of Zenker’s peroral endoscopic myotomy (Z-POEM) for treatment of Zenker’s diverticulumEndosc Int Open 2023; 11(06): E607-E612DOI: 10.1055/a-2067-9105 Comment on: A 3D-printed pedal fixator for connecting different pedal-operated tools reduces the number of mistakes during endoscopic submucosal dissectionEndosc Int Open 2023; 11(07): E635-E640DOI: 10.1055/a-2095-0197
PDE4D mediates impaired β-adrenergic receptor signalling in the sinoatrial node in mice with hypertensive heart disease
Authors: Tristan W Dorey, Megan D McRae, Darrell D Belke, Robert A Rose
Journal: Cardiovascular Research (2023)

Abstract Aims The sympathetic nervous system increases HR by activating β-adrenergic receptors (β-ARs) and increasing cAMP in sinoatrial node (SAN) myocytes while phosphodiesterases (PDEs) degrade cAMP. Chronotropic incompetence, the inability to regulate heart rate (HR) in response to sympathetic nervous system activation, is common in hypertensive heart disease; however, the basis for this is poorly understood. The objective of this study was to determine the mechanisms leading to chronotropic incompetence in mice with angiotensin II (AngII)-induced hypertensive heart disease. Methods and results C57BL/6 mice were infused with saline or AngII (2.5 mg/kg/day for 3 weeks) to induce hypertensive heart disease. HR and SAN function in response to the β-AR agonist isoproterenol (ISO) were studied in vivo using telemetry and electrocardiography, in isolated atrial preparations using optical mapping, in isolated SAN myocytes using patch-clamping, and using molecular biology. AngII-infused mice had smaller increases in HR in response to physical activity and during acute ISO injection. Optical mapping of the SAN in AngII-infused mice demonstrated impaired increases in conduction velocity and altered conduction patterns in response to ISO. Spontaneous AP firing responses to ISO in isolated SAN myocytes from AngII-infused mice were impaired due to smaller increases in diastolic depolarization (DD) slope, hyperpolarization-activated current (If), and L-type Ca2+ current (ICa,L). These changes were due to increased localization of PDE4D surrounding β1- and β2-ARs in the SAN, increased SAN PDE4 activity, and reduced cAMP generation in response to ISO. Knockdown of PDE4D using a virus-delivered shRNA or inhibition of PDE4 with rolipram normalized SAN sensitivity to β-AR stimulation in AngII-infused mice. Conclusions AngII-induced hypertensive heart disease results in impaired HR responses to β-AR stimulation due to up-regulation of PDE4D and reduced effects of cAMP on spontaneous AP firing in SAN myocytes.
The First Crested Duck Genome Reveals Clues to Genetic Compensation and Crest Cushion Formation
Authors: Guobin Chang, Xiaoya Yuan, Qixin Guo, Hao Bai, Xiaofang Cao, Meng Liu, Zhixiu Wang, Bichun Li, Shasha Wang, Yong Jiang, Zhiquan Wang, Yang Zhang, Qi Xu, Qianqian Song, Rui Pan, Lingling Qiu, Tiantian Gu, Xinsheng Wu, Yulin Bi, Zhengfeng Cao, Yu Zhang, Yang Chen, Hong Li, Jianfeng Liu, Wangcheng Dai, Guohong Chen
Journal: Genomics Proteomics & Bioinformatics (2023)

Abstract The Chinese crested (CC) duck is a unique indigenous waterfowl breed, which has a crest cushion that affects its survival rate. Therefore, the CC duck is an ideal model to investigate the genetic compensation response to maintain genetic stability. In the present study, we first generated a chromosome-level genome of CC ducks. Comparative genomics revealed that genes related to tissue repair, immune function, and tumors were under strong positive selection, indicating that these adaptive changes might enhance cancer resistance and immune response to maintain the genetic stability of CC ducks. We also assembled a Chinese spot-billed (Csp-b) duck genome, and detected the structural variations (SVs) in the genome assembl ies of three ducks (i.e., CC duck, Csp-b duck, and Peking duck). Functional analysis revealed that several SVs were related to the immune system of CC ducks, further strongly suggesting that genetic compensation in the anti-tumor and immune systems supports the survival of CC ducks. Moreover, we confirmed that the CC duck originated from the mallard ducks. Finally, we revealed the physiological and genetic basis of crest traits and identified a causative mutation in TAS2R40 that leads to crest formation. Overall, the findings of this study provide new insights into the role of genetic compensation in adaptive evolution.
Tumor Treating Fields therapy with standard systemic therapy versus standard systemic therapy alone in metastatic non-small-cell lung cancer following progression on or after platinum-based therapy (LUNAR): a randomised, open-label, pivotal phase 3 study
Authors: Ticiana Leal, Rupesh Kotecha, Rodryg Ramlau, Li Zhang, Janusz Milanowski, Manuel Cobo, Jaromir Roubec, Lubos Petruzelka, Libor Havel, Sujith Kalmadi, Jeffrey Ward, Zoran Andric, Thierry Berghmans, David E Gerber, Goetz Kloecker, Rajiv Panikkar, Joachim Aerts, Angelo Delmonte, Miklos Pless, Richard Greil, Christian Rolfo, Wallace Akerley, Michael Eaton, Mussawar Iqbal, Corey Langer
Journal: The Lancet Oncology (2023)
Combined cytotoxic and immune-stimulatory gene therapy for primary adult high-grade glioma: a phase 1, first-in-human trial
Authors: Yoshie Umemura, Daniel Orringer, Larry Junck, Maria L Varela, Molly E J West, Syed M Faisal, Andrea Comba, Jason Heth, Oren Sagher, Denise Leung, Aaron Mammoser, Shawn Hervey-Jumper, Daniel Zamler, Viveka N Yadav, Patrick Dunn, Wajd Al-Holou, Todd Hollon, Michelle M Kim, Daniel R Wahl, Sandra Camelo-Piragua, Andrew P Lieberman, Sriram Venneti, Paul McKeever, Theodore Lawrence, Ryo Kurokawa, Karen Sagher, David Altshuler, Lili Zhao, Karin Muraszko, Maria G Castro, Pedro R Lowenstein
Journal: The Lancet Oncology (2023)
Neoadjuvant palbociclib plus either giredestrant or anastrozole in oestrogen receptor-positive, HER2-negative, early breast cancer (coopERA Breast Cancer): an open-label, randomised, controlled, phase 2 study
Authors: Sara A Hurvitz, Aditya Bardia, Vanesa Quiroga, Yeon Hee Park, Isabel Blancas, José Luis Alonso-Romero, Aleksandr Vasiliev, Hryhoriy Adamchuk, Marcelo Salgado, Denise A Yardley, Oleksandr Berzoy, Pilar Zamora-Auñón, David Chan, Gonzalo Spera, Cloris Xue, Erika Ferreira, Tanja Badovinac Crnjevic, Pablo Diego Pérez-Moreno, Vanesa López-Valverde, Jutta Steinseifer, Tharu M Fernando, Heather M Moore, Peter A Fasching
Journal: The Lancet Oncology (2023)
Deep submucosal invasion as a risk factor for recurrence after endoscopic submucosal dissection for T1 colorectal cancer
Authors: João Santos-Antunes, Frieder Berr, Mathieu Pioche, Felipe Ramos-Zabala, Paolo Cecinato, Francisco Gallego, Pedro Barreiro, Catarina Félix, Sandro Sferrazza, Andrej Wagner, Arnaud Lemmers, Mariana Figueiredo Ferreira, Eduardo Albéniz, Ricardo Küttner-Magalhães, Carlos Fernandes, Rui Morais, Sunil Gupta, Daniel Martinho-Dias, Elisabete Rios, Isabel Faria-Ramos, Margarida Marques, Michael J. Bourke, Guilherme Macedo
Journal: Endoscopy (2023)

See also: Pathologic sm2 carries a moderate risk of metastases even without other unfavorable factors, but positive horizontal margins have low local recurrence risk after en bloc resectionEndoscopy 2023; 55(03): 252-254DOI: 10.1055/a-1996-0826 See also: Reply to Santos-Antunes et al.Endoscopy 2023; 55(09): 883-883DOI: 10.1055/a-2082-8116
Phase II Trial of Dabrafenib Plus Trametinib in Relapsed/Refractory <i>BRAF</i> V600–Mutant Pediatric High-Grade Glioma
Authors: Darren R. Hargrave, Keita Terashima, Junichi Hara, Uwe R. Kordes, Santhosh A. Upadhyaya, Felix Sahm, Eric Bouffet, Roger J. Packer, Olaf Witt, Larissa Sandalic, Agnieszka Kieloch, Mark Russo, Kenneth J. Cohen, Blanca Diez, Andrea Cappellano, Sidnei Epelman, Bruna Mancano, Karsten Nysom, Isabelle Aerts, Anne-Isabelle Bertozzi, Olaf Witt, Christof Kramm, Gudrun Fleischhack, Uwe Kordes, Pablo Hernaiz-Driever, Maura Massimino, Maria Luisa Garre, Franco Locatelli, Keita Terashima, Keiko Okada, Yuki Koga, Jasper Van der Lugt, Alexey Maschan, Alvaro Lassaletta, Stefan Holm, Darren Hargrave, Lisa Howell, Santhosh Upadhyaya, Karen Gauvain, Kenneth Cohen, Patricia Baxter
Journal: Journal of Clinical Oncology (2023)

PURPOSE BRAF V600 mutation is detected in 5%-10% of pediatric high-grade gliomas (pHGGs), and effective treatments are limited. In previous trials, dabrafenib as monotherapy or in combination with trametinib demonstrated activity in children and adults with relapsed/refractory BRAF V600–mutant HGG. METHODS This phase II study evaluated dabrafenib plus trametinib in patients with relapsed/refractory BRAF V600–mutant pHGG. The primary objective was overall response rate (ORR) by independent review by Response Assessment in Neuro-Oncology criteria. Secondary objectives included ORR by investigator determination, duration of response (DOR), progression-free survival, overall survival (OS), and safety. RESULTS A total of 41 pediatric patients with previously treated BRAF V600–mutant HGG were enrolled. At primary analysis, median follow-up was 25.1 months, and 51% of patients remained on treatment. Sixteen of 20 discontinuations were due to progressive disease in this relapsed/refractory pHGG population. Independently assessed ORR was 56% (95% CI, 40 to 72). Median DOR was 22.2 months (95% CI, 7.6 months to not reached [NR]). Fourteen deaths were reported. Median OS was 32.8 months (95% CI, 19.2 months to NR). The most common all-cause adverse events (AEs) were pyrexia (51%), headache (34%), and dry skin (32%). Two patients (5%) had AEs (both rash) leading to discontinuation. CONCLUSION In relapsed/refractory BRAF V600–mutant pHGG, dabrafenib plus trametinib improved ORR versus previous trials of chemotherapy in molecularly unselected patients with pHGG and was associated with durable responses and encouraging survival. These findings suggest that dabrafenib plus trametinib is a promising targeted therapy option for children and adolescents with relapsed/refractory BRAF V600–mutant HGG.
Methyl Donor Nutrient Intake and Incidence of Type 2 Diabetes: Results From Three Large U.S. Cohorts
Authors: Caleigh M. Sawicki, Danielle E. Haslam, Kim V.E. Braun, Jean-Philippe Drouin-Chartier, Trudy Voortman, Oscar H. Franco, Qi Sun, Frank B. Hu, Shilpa N. Bhupathiraju
Journal: Diabetes Care (2023)

We examined whether intake of methyl donor nutrients, including vitamins B2, B6, and B12 and folate, from foods and/or supplements is associated with type 2 diabetes risk.